左旋多巴诱导异动症大鼠模型纹状体棘状神经元电活动的研究

目的研究左旋多巴诱导异动症(levodopa induced-dyskinesias LID)大鼠模型纹状体棘状神经元的自发性电活动变化。方法帕金森病(Parkinson disease PD)大鼠模型应用左旋多巴(L-dopa)治疗28d诱发LID大鼠模型,29d L-dopa治疗前15min腹腔注射N-methyl-D-aspartic acid(NMDA)受体拮抗剂地佐环平(MK-801)1次。采用微电极细胞外记录技术检测大鼠模型纹状体棘状神经元的电生理活动。结果LID大鼠纹状体神经元的自发性电活动较对照组(P<0.01)及PD组(P<0.05)明显增多,MK-801治疗后显著减少(P<0.01)。结论纹状体棘状神经元的自发性电活动改变是LID的重要发病机制之一,NMDA受体拮抗剂可能通过逆转纹状体棘状神经元的电活动抑制LID的发生。

Electrophysiological characteristics on striatal medium-spiny neurons in rats with levodopa induced-dyskinesias

Objective To study the striatal spontaneous electrophysiological characteristics in rats with levodopa induced-dyskinesia. Methods PD rats were treated with chronic intermittent L-dopa by celiac injection for 28 days to get the LID rats. On 29d,the animals were given an acute administration of MK-801 15 min prior levodopa treatment. Electrophysiological characteristics were studied by extracellular recording in PD,LID and control rats. Results Spontaneous firing rates in striatum of LID group were more than control group(P< 0.01 )and PD group(P< 0.05 )significantly. They decreased markedly in MK-801 treatment group compared with LID group(P< 0.01 ). Conclusion The change of spontaneous electrophysiological characteristics of striatal neurons in rat is one of the causes of levodopa induced-dyskinesia. Glutamate receptor blockade may prevent occurrence of LID through reversing activity of striatal neurons.